A pathogenic bacterium triggers epithelial signals to form a functional bacterial receptor that mediates actin pseudopod formation

被引:220
作者
Rosenshine, I
Ruschkowski, S
Stein, M
Reinscheid, DJ
Mills, SD
Finlay, BB
机构
[1] UNIV BRITISH COLUMBIA, BIOTECHNOL LAB, VANCOUVER, BC V6T 1Z3, CANADA
[2] UNIV BRITISH COLUMBIA, DEPT BIOCHEM & MOLEC BIOL, VANCOUVER, BC V6T 1Z3, CANADA
[3] UNIV BRITISH COLUMBIA, DEPT MICROBIOL & IMMUNOL, VANCOUVER, BC V6T 1Z3, CANADA
[4] HEBREW UNIV JERUSALEM, FAC MED, DEPT BIOTECHNOL & MOL GENET, IL-91120 JERUSALEM, ISRAEL
关键词
actin; diarrhea; enteropathogenic Escherichia coli; pathogenesis; signal transduction;
D O I
10.1002/j.1460-2075.1996.tb00621.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Enteropathogenic E. coli (EPEC) belongs to a group of bacterial pathogens that induce actin accumulation beneath adherent bacteria. We found that EPEC adherence to epithelial cells mediates the formation of fingerlike pseudopods (up to 10 mu m) beneath bacteria. These actin-rich structures also contain tyrosine phosphorylated host proteins concentrated at the pseudopod tip beneath adherent EPEC. Intimate bacterial adherence (and pseudopod formation) occurred only after prior bacterial induction of tyrosine phosphorylation of an epithelial membrane protein, Hp90, which then associates directly with an EPEC adhesin, intimin. These interactions lead to cytoskeletal nucleation and pseudopod formation. This is the first example of a bacterial pathogen that triggers signals in epithelial cells which activates receptor binding activity to a specific bacterial ligand and subsequent cytoskeletal rearrangement.
引用
收藏
页码:2613 / 2624
页数:12
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